The bacteria Streptococcus pneumoniae harmlessly colonizes the mucous linings of throats and noses in most people, only becoming virulent when they leave those comfortable surroundings and enter the middle ears, lungs or bloodstream. Now, in research published in July in mBio, University at Buffalo researchers reveal how that happens.
We were asking, what is the mechanism behind what makes us sick? explains Anders P. Hakansson, PhD, assistant professor of microbiology and immunology in the UB School of Medicine and Biomedical Sciences. We are looking to find ways to interfere with the transition to disease. Few have looked at the specific mechanism that suddenly makes these bacteria leave the nose where they typically prefer to reside and travel into the lungs or the middle ear where they cause disease. If we can understand that process, then maybe we can block it.
Hakansson and his colleagues had previously found that when the pneumococci colonize the nose, they form sophisticated, highly structured biofilm communities.
In the current study, the research team grew biofilms of pneumococci on top of human epithelial cells, where the bacteria normally grow. They then infected these bacteria with influenza A virus or exposed them to the conditions that typically accompany the flu, including increased temperature to mimic fever, increased concentrations of ATP (the energy molecule in cells), and the stress hormone norepinephrine, released during flu infection.
All three stimuli triggered a sudden release and departure of bacteria from the biofilm in the nose into otherwise normally sterile organs, such as the middle ears and lungs or into the bloodstream. At the same time, the researchers found that the gene expression profile of the bacteria that had dispersed from the biofilms revealed far more virulence.
Â
Hakansson says the research demonstrates how the mammalian and bacterial kingdoms interact. Humans are the only natural hosts for these bacteria, he explains, when the viral infection comes in, there is this interkingdom signaling, where the bacteria respond to host molecules. If we can find ways to interrupt that signaling, we might be able to prevent disease.
Hakansson is affiliated with the Witebsky Center for Microbial Pathogenesis and Immunology and the New York State Center of Excellence in Bioinformatics and Life Sciences, both at UB. The major portion of the work was conducted by co-author Laura R. Marks, an MD/PhD candidate in the UB Department of Microbiology and Immunology, with co-authors Bruce A. Davidson, research assistant professor of anesthesiology and Paul R. Knight, III, MD, PhD, professor of anesthesiology and microbiology and immunology.
The work was funded by the UB Department of Microbiology and Immunology.
Source: University at Buffalo
A Helping Hand: Innovative Approaches to Expanding Hand Hygiene Programs in Acute Care Settings
July 9th 2025Who knew candy, UV lights, and a college kid in scrubs could double hand hygiene adherence? A Pennsylvania hospital’s creative shake-up of its infection prevention program shows that sometimes it takes more than soap to get hands clean—and keep them that way.
Broadening the Path: Diverse Educational Routes Into Infection Prevention Careers
July 4th 2025Once dominated by nurses, infection prevention now welcomes professionals from public health, lab science, and respiratory therapy—each bringing unique expertise that strengthens patient safety and IPC programs.
How Contaminated Is Your Stretcher? The Hidden Risks on Hospital Wheels
July 3rd 2025Despite routine disinfection, hospital surfaces, such as stretchers, remain reservoirs for harmful microbes, according to several recent studies. From high-touch areas to damaged mattresses and the effectiveness of antimicrobial coatings, researchers continue to uncover persistent risks in environmental hygiene, highlighting the critical need for innovative, continuous disinfection strategies in health care settings.